Various types of electrical stimulation have been known to be used for various therapeutic purposes for millennia, tracing all the way back to Roman times when physicians treated patients suffering from pain and acute gout with electric rays and other electrically-charged sea creatures. Since that time, many medical uses for electrical stimulation have been developed, with one of the most important and prevalent uses in modern times being embodied in cardiac pacemakers.
Cardiac pacemakers stimulate cardiac activity in a patient by delivering periodic electrical pulses through electrodes to the patient's heart. The electrical pulses cause electrical depolarization and subsequent cardiac contraction to assist the heart in beating at a desired rhythm. There are many different varieties of cardiac pacemaker systems. In general, cardiac pacemaker systems are categorized according to the location of the electrodes and the pathway that the electrical stimulus travels to the heart.
The earliest wearable pacemakers were “epicardial” pacing systems, wherein electrodes are placed on the surface of the heart. While these types of pacemakers are still in widespread use in certain circumstances, other types of pacemakers have also been developed and widely used. For example, “transvenous” pacemaker systems use electrodes mounted on catheters that are maneuvered through large central veins to the right ventricle or right atrium of the heart, while “transesophageal” pacing systems employ electrodes located in the esophagus. Another type of pacemaker is the “transcutaneous” cardiac pacemaker system, which delivers pacing impulses to the heart through the patient's skin using cutaneous electrodes (i.e., electrodes externally attached to the skin of the patient).
The present invention invention concerns the transcutaneous type of cardiac pacing systems, as well as other types of transcutaneous cardiac treatment systems not related to pacing.
Transcutaneous pacing is commonly used in emergency medicine for immediate treatment of unstable bradycardia, a condition in which the heart is beating too slowly and/or irregularly. Since the electrodes are attached externally to the skin, the transcutaneous pacing can be applied immediately to a heart troubled patient without intervention, and thereby have traditionally served as a therapeutic bridge until a transvenous or other type of implantable pacemaker could be established under more controlled circumstances.
One of the drawbacks with traditional transcutaneous pacing, however, is that patients may experience discomfort. More specifically, the discomfort may be in the form of a muscular skeletal pain induced from electrical skin and muscle stimulation. Depending upon the patient's own tolerance level and the current required for rhythm capture in the specific situation, this discomfort might range from moderate and tolerable to severe and intolerable. Typically, the applied current will be set at 10 milliamps to start and then be increased by increments of 10 until rhythm capture is noted. At that point, the pacing system current will then typically be set at a current of about 1.25 times what was required for capture. It has been found that most patients cannot tolerate currents of 50 milliamps and higher without sedation, while often 50-100 milliamps are required. Thus, practitioners are encouraged to strongly consider sedation in connection with traditional transcutaneous pacing systems, and even then, with long term use, burns are not uncommon.
While the relatively high direct currents necessary for pacing using traditional transcutaneous pacemakers may be unavoidable in some situations (e.g., where there is serious damage to the electrical systems of the heart), there are other situations where such high currents may not be required. For example, in cases of ventricular tachycardia, the heart may beat very rapidly and inefficiently (for example at a rate of 150 beats per minute or more). Moreover, it is known that arrhythmic ventricular fibrillation often occurs in a fatal heart attacks, and it may be desirable to specifically treat this condition instead of or in addition to the application of a direct current shock from a defibrillator.
In such situations involving arrhythmias, it has been found that stimulation of the cardiac branches of the vagus nerve may allow for the desired results to be achieved. The vagus nerve, which is the main parasympathetic nerve of the body and is outside of the spinal cord, regulates heart rate. Increased vagal activity slows the heart down. Thus, through secondary effect on the cardiac branches of the vagus nerve as opposed to direct effect on the SA and AV nodes, cardiac rhythm may be slowed, for example, in ventricular tachycardia, from an inefficient 150 beats per minute down to 60 beats per minute as part of initial treatment by the cardiologist.
A similar approach can be used to slow down the arrhythmic ventricular fibrillation that often occurs in a fatal heart attack to perhaps augment a direct current shock from a defibrillator by keeping the heart rate slow and controlled so as not to have to re-shock the patient, thereby employing not only direct electrical stimulation of the heart muscle itself, but also employing vagus nerve control of the heart.
Another similar approach is to affect the muscular contracture to the atrium in order to treat atrial fibrillation on a short term basis acting as a temporary substitute or bridge until a regular pacemaker can be inserted.
What is desired, therefore, is an external cardiac pacing system that may be used in certain appropriate situations instead of or in addition to traditional transcutaneous pacemaker systems, that can be applied immediately to a heart troubled patient, but that does not suffer from the disadvantages of such traditional systems (i.e., causing discomfort, thereby often necessitating sedation, and possibly causing skin damage).
Also desired is a replacement for other cardiac treatment systems that require surgical implantation of leads, with consequently similar disadvantages, as compared to implantable cardiac pacemaker systems.
For example, research and development is currently underway to alleviate problems associated with heart failure using electrical stimulation by way of a technique known as cardiac contractility modulation (CCM). The short- and long-term use of this therapy has been found to enhance the strength of ventricular contraction and therefore the heart's pumping capacity by modulating (adjusting) the myocardial contractility.
More specifically, in CCM therapy, electrical stimulation is applied to the cardiac muscle during the absolute refractory period. In this phase of the cardiac cycle, electrical signals cannot trigger new cardiac muscle contractions, hence this type of stimulation is known as a non-excitatory stimulation. However, the electrical signals increase the influx of calcium ions into the cardiac muscle cells (cardiomyocytes). In contrast to other electrical stimulation treatments for heart failure, such as pacemaker therapy or implantable cardioverter defibrillators, CCM does not affect the cardiac rhythm directly. Rather, the aim is to enhance the heart's natural contraction (the native cardiac contractility) sustainably over long periods of time. Furthermore, unlike most interventions that increase cardiac contractility, CCM is not associated with an unfavorable increase in oxygen demand by the heart. This may be explained by the beneficial effect the therapy has in improving cardiac efficiency.
A meta-analysis in 2014 and an overview of device-based treatment options in heart failure in 2013 concluded that CCM treatment is safe, that it is generally beneficial to patients and that the treatment increases the exercise tolerance and quality of life of patients. Furthermore, preliminary long-term survival data shows that CCM treatment is associated with lower long-term mortality in heart failure patients when compared with expected rates among similar patients not treated with CCM.
However, traditional CCM treatment options do suffer from disadvantages, which disadvantages are similar to those associated with traditional pacemakers. Specifically, traditional CCM treatment options involve either the surgical placement of leads on or in the heart, or involve the application of relatively high current transcutaneously, which can cause patient discomfort, thereby possibly necessitating sedation, and which can cause skin damage.
Thus, what is also desired, is an external CCM treatment system that maintains the benefits of traditional CCM treatment systems, but that does not suffer from the disadvantages of such traditional systems (i.e., either requiring surgical intervention in the case of implantable systems or causing discomfort, thereby often necessitating sedation, and possibly causing skin damage in the case of transcutaneous systems).
Similarly, cardiac ultrasounds are often used to noninvasively identify ventricular wall inappropriate contraction or lack of contraction, signifying a prior myocardial infarction where the muscle is now no longer working correctly. An external treatment system is desired that can be used to stimulate blood flow to scarred or devitalized cardiac tissue to help the muscle that is still alive to contract in a more normal fashion with the rest of the ventricle. Similarly, such stimulation of blood flow to an area of marginally compromised but not yet devitalized cardiac muscle would help muscle in that situation to heal more effectively and with less malfunctioning scar tissue. The increased circulation provided by the invention can also be utilized to help stimulate and promote an environment conducive to stem cell survival or to successful implementation of other alternative treatments currently being investigated to grow new cardiac tissue in damaged areas of the heart.
Further desired is an external cardiac treatment system that may be used to assist in the treatment of ischemic heart disease, angina, and consequences from acute myocardial infarction. Such a system is also desired to be used in connection with assisting with cardiac stenting and promoting better outcomes for treatment of stenosed coronary arteries.
Millions of EKGs are done in doctor's offices on a daily basis as a screening test for coronary artery disease and ischemic heart disease to pre-emptively identify these situations and treat them before there is a myocardial infarction and actual cardiac muscle death, dysfunction, and congestive heart failure, or death from a myocardial infarction.
One of the ways that angina and ischemic heart disease is treated, when present on a chronic or crescendo basis over time, is with sublingual nitroglycerin, which is a coronary artery vasodilator, and also decreases “afterload” on the heart in terms of left ventricular pumping. This makes it easier for the heart to pump at a lower blood pressure because of vasodilatation from the aorta distally in terms of pushback or resistance from vascular abnormal afterload. Afterload is a term commonly used to describe arteriosclerotic vascular disease and hypertension as conditions either independent of each other or found in combination with each other, that force the heart to pump more aggressively at a higher blood pressure in order to deliver blood to the rest of the body. By decreasing the afterload with nitroglycerine, or any type of antihypertensive pharmacologic agent, this increased workload for the heart is diminished on a temporary basis, allowing the heart to get more oxygen, work less hard, and hopefully diminish the pain and symptoms associated with angina while protecting the heart from a myocardial infarction and cell death.
However, it should be noted that all of the medications used to treat acute myocardial infarctions and ischemic heart disease in acute and chronic stages, such as antihypertensive medications and medications that decrease afterload, have associated pharmacological side effects that can potentially be life threatening in their own right.
Screening EKGs in doctor's offices are used to see if there is an area of the heart that is ischemic, even though there may not be symptomatology from it. This is reflected in an inverted T-wave in any one of the EKG leads. When a cardiologist notes a new inverted T-wave or change in a patient's EKG taken as a diagnostic screening measure, he/she needs to assess the status of the coronary artery that goes to the area of the heart that correlates anatomically with the abnormal EKG, and to consider performing a cardiac catheterization to determine if there is a stenosis serious enough to result in, or evolve into, a life threatening situation. Depending on the data from the EKG and the more advanced and invasive medical work up of the situation, the cardiologist must consequently determine whether a stent or pharmacologic treatments or a combination of both, as described above, will help.
It would be desirable to be able target the ischemic area of the heart identified by the inverted T-wave on EKG and other diagnostic studies, for vasodilatation treatment in order to increase blood flow to that particular ischemic area on a small vessel basis, and even target whichever major coronary artery that supplies the identified area, treating it with transcutaneous electrical stimulation while waiting for a stent to be placed. Targeting the stenotic area of a main coronary artery with transcutaneous electrical stimulation to cause it to vasodilate would allow for protection of the heart while treatment is undertaken. Such a system may be used in conjunction with various pharmacologic agents so as to work synergistically with those agents to decrease cardiac afterload, or it would provide treatment during the time frame waiting for such medications to take effect, or in some cases, such a system may be used instead of pharmacologic agents to avoid deleterious side effects.